Elevated levels of serum IL-5 are associated with an increased likelihood of major depressive disorder
1 Department of Psychiatry, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland
2 Central Hospital of Central Finland, Jyväskylä, and University of Eastern Finland, Kuopio, Finland
3 Institute of Biomedicine, Division of Physiology and Biocenter Oulu, University of Oulu, Finland
4 Department of Clinical Medicine, University of Oulu, Finland
5 Department of Psychiatry, Lapland Hospital District, Rovaniemi, Finland
6 Kuopio Psychiatric Center, Kuopio, Finland
7 Department of Dermatology, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland
BMC Psychiatry 2012, 12:2 doi:10.1186/1471-244X-12-2Published: 9 January 2012
Inflammatory mediators in both the peripheral circulation and central nervous system (CNS) are dysregulated in major depressive disorder (MDD). Nevertheless, relatively little is known about the role of the T-helper (Th)-2 effector cytokines interleukin (IL)-5 and IL-13 in MDD.
We examined the serum levels of these cytokines and a Th-1 comparison cytokine, interferon (IFN)-γ, in 116 individuals (MDD, n = 58; controls, n = 58).
In our basic multivariate model controlling for the effects of potential confounders on the associations between MDD and the examined cytokines, each 1-unit increase in the serum IL-5 level increased the likelihood of belonging to the MDD group by 76% (OR 1.76, 95% CI 1.03-2.99, p = 0.04; model covariates: age, gender, marital status, daily smoking and alcohol use). The likelihood further increased in models additionally controlling for the effects of the use of antidepressants and NSAIDS, and a diagnosis of asthma. No such associations were detected with regard to IL-13 (OR 1.08, 95% CI 0.96-1.22, p = 0.22) or IFN-γ (OR 1.02, 95% CI 0.99-1.05, p = 0.23).
Elevated levels of IL-5, which uses the neural plasticity-related RAS GTPase-extracellular signal-regulated kinase (Ras-ERK) pathway to mediate its actions in the central nervous system (CNS), could be one of the factors underlying the depression-related changes in CNS plasticity.